GLP-1 Agonists Exendin-4 Protection Of GSIS Min6 Cells And The Role Of MAPK Signal Pathway

objectiveTo investigate under effects of MAPK signaling pathway by IL-1β, via Exendin-4 treated, effect on GSIS and the change of MAPK singal pathway. Methods (1) min6 cells were incubated in KRBH buffer containing 0,5.5, 11.1,22.2mmol/1 glucose for 60 mins. Collecting supernatant and protein,insulin asssus by ELISA,cell lysate was used for Western bliot to test the levels of phosphorylated MAPK (ERK1/2, P38, JNK) and β-actin. (2) min6 cells were incubated in DMEM containing IL-1β (0、0.25、2.5ng/ml) for 24 hour.DMEM was then replaced with fresh KRB buffercontaining 22.2 mmol/1 glucose for 60 mins. Collecting supernatant and protein,insulin asssus by ELISA,cell lysate was used for Western bliot to test the levels of phosphorylated MAPK (ERK 1/2, P38, JNK) and β-actin.(3) min6 cells were incubated in DMEM containing 0.25ng/ml IL-1β and Exendin-4 (50、500pmol/ml) for 24 hours. DMEM was then replaced with fresh KRB buffercontaining 22.2 mmol/1 glucose for 60 mins. Collecting supernatant and protein,insulin asssus by ELISA,cell lysate was used for Western bliot to test the levels of phosphorylated MAPK (ERK1/2, P38, JNK) and β-actin.Results (1) IL-1β inhibited GSIS in min6 cells, down-regulated the phosphorylated of ERK up-regulated the phosphorylated of p38 and JNK. (2) The damage caused by IL-1β to Exendin-4 has a protective effect on GSIS in min6 cells,and up-regulated the phosphorylated of ERK1/2, down-regulated the phosphorylated of JNK. Conclusion Exendin-4 to GSIS of protection could be reached by MAPK Signaling Pathway.